{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T22:08:37Z","timestamp":1769724517112,"version":"3.49.0"},"reference-count":44,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,3,25]],"date-time":"2013-03-25T00:00:00Z","timestamp":1364169600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2013,8]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Alcohol abuse is the second leading cause of dilated cardiomyopathy, a disorder specifically referred to as alcoholic cardiomyopathy (<jats:styled-content style=\"fixed-case\">ACM<\/jats:styled-content>). Rodent and human studies have revealed cardiac fibrosis to be a consequence of <jats:styled-content style=\"fixed-case\">ACM<\/jats:styled-content>, and prior studies by this laboratory have associated this occurrence with elevated transforming growth factor\u2010beta (<jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2) and activated fibroblasts (myofibroblasts). To date, there have been no other studies to investigate the direct effect of alcohol on the cardiac fibroblast.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Primary rat cardiac fibroblasts were cultured in the presence of ethanol (<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>t<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>) and assayed for fibroblast activation by collagen gel contraction, alpha\u2010smooth muscle actin (\u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>) expression, migration, proliferation, apoptosis, collagen <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 expression. The <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 receptor type 1 inhibitor compound <jats:styled-content style=\"fixed-case\">SB<\/jats:styled-content> 431542 and a soluble recombinant <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> receptor (Rb<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>) were used to assess the role of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 in the response of cardiac fibroblasts to <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>t<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Treatment for cardiac fibroblasts with <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>t<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> at concentrations of 100\u00a0mg\/dl or higher resulted in fibroblast activation and fibrogenic activity after 24\u00a0hours including an increase in contraction, \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content> expression, migration, and expression of collagen <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2. No changes in fibroblast proliferation or apoptosis were observed. Inhibition of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 by <jats:styled-content style=\"fixed-case\">SB<\/jats:styled-content> 431542 and Rb<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> attenuated the <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>t<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>\u2010induced fibroblast activation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>EtOH treatment directly promotes cardiac fibroblast activation by stimulating <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 release from fibroblasts. Inhibiting the action of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 decreases the fibrogenic effect induced by <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>t<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> treatment. The results of this study support <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 to be an important component in cardiac fibrosis induced by exposure to <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>t<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12111","type":"journal-article","created":{"date-parts":[[2013,3,25]],"date-time":"2013-03-25T16:09:24Z","timestamp":1364227764000},"page":"1286-1294","source":"Crossref","is-referenced-by-count":27,"title":["Activation of Cardiac Fibroblasts by Ethanol Is Blocked by <scp>TGF<\/scp>\u2010\u03b2 Inhibition"],"prefix":"10.1111","volume":"37","author":[{"given":"Brittany A.","family":"Law","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Anatomy  University of South Carolina School of Medicine Columbia South Carolina"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wayne 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